Myeloid Bmal1 deletion increases monocyte recruitment and worsens atherosclerosis.

ABSTRACT: BMAL1, the nonredundant transcription factor in the core molecular clock, has been implicated in cardiometabolic diseases in mice and humans. BMAL1 controls the cyclic trafficking of Ly6c^hi monocytes to sites of acute inflammation. Myeloid deficiency of Bmal1 also worsens chronic inflammation in diet-induced obesity. We studied whether myeloid Bmal1 deletion promotes atherosclerosis by enhancing monocyte recruitment to atherosclerotic lesions. By generating Bmal1^FloxP/FloxP;LysM^Cre mice on the Apoe^-/- background, we showed that Bmal1 deletion in myeloid cells increased the size of atherosclerotic lesions. Bmal1 deficiency in monocytes and macrophages resulted in an increased total number of lesional macrophages

SUBMITTER: Huo M 

PROVIDER: S-EPMC6191064 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature